The present invention relates generally to implantable cardiac stimulation devices. The present invention more particularly relates to methods and devices for multi-chamber anti-tachycardia pacing.
The heart is a series of pumps that are carefully controlled by a very special electrical system. This electrical system attempts to regulate the heart rate between 60 and 100 beats per minute. The initial electrical signal originates near the top of the upper chamber on the right side of the heart.
This chamber is called the xe2x80x9cright atriumxe2x80x9d and the special tissue that generates the signal is called the xe2x80x9csino-atrialxe2x80x9d or SA node.
The electrical signal continues in a downward fashion through the xe2x80x9catrio-ventricularxe2x80x9d or AV node, where the signal is slowed slightly by special tissue. The AV node is the xe2x80x9cdoorwayxe2x80x9d or relay station to the bundle of His (pronounced Hiss), and the bundle branches in the lower chambers of the heart.
After passing through the left and right bundle branches, the impulse arrives at the Purkinje fibers, where it is transmitted to the muscle cells of the left and right ventricles. Because of the specialized way in which the impulse is transmitted, the ventricles contract almost simultaneously.
With normal conduction, the cardiac contractions are very organized and timed so that the top chambers (the atria) contract before the lower chambers and the heart rate is maintained between 60 and 100 beats per minute.
Abnormally fast heart rates are called tachycardias. As used herein, the term tachycardia means a heartbeat at a rate which is abnormally high and accordingly considered to be dangerous if permitted to continue, or any arrhythmia involving recognizable heartbeat patterns containing repetitions which are in excess of a periodic heartbeat within a safe range.
When the ventricular chambers beat too quickly, the arrhythmia (i.e., unusual heart rhythm) is known as ventricular tachycardia. When ventricular tachycardia (VT) occurs, the ventricles may not be able to fill with enough blood to supply the body with the oxygen rich blood that it needs. Symptoms of VT include feeling faint, sometimes passing out, dizzyness, or a pounding in the chest.
Ventricular tachycardia may be controlled by medication in some cases. If medications are not effective, the physician may elect to control the rhythm by electrical methods. The most common electrical therapy for VT is implantation of a device known as an Implantable Cardioverter Defibrillator (ICD). The ICD applies an electric shock to the heart muscle to interrupt or disrupt the fast rhythm. The electric shock may be in the form of specially timed pacemaker pulses (unfelt by the patient) or by high voltage shock. The high voltage shock, if required, is usually painful to the patient. Accordingly, it is preferential to use pacemaker pulses (also referred to as pacing pulses).
Tachycardias can result due to any number of reasons. For example, patients who have had myocardial infarctions, or other diseases that create scarring in the ventricular region of the heart, often develop monomorphic ventricular tachycardias. A monomorphic ventricular tachycardia (MVT) is a type of tachycardia that originates from one ventricular focus. These tachycardias often arise in and around the area of scarring on the heart. They are typically uniform and typically occur at a regular rate. Faster MVTs are often associated with hemodynamic compromise, whereas slower MVTs can be very stable.
Anti-Tachycardia Pacing (ATP) has been used to convert ventricular tachycardias into normal sinus rhythm. However, conventional ATP has not proved to be one hundred percent successful at returning the heart to normal sinus rhythm. Additionally, in a rare case, conventional ATP will accelerate the rhythm to ventricular fibrillation. Accordingly, improved methods and apparatuses for decreasing the failure rate of ATP are required. Some of the prior patent documents which teach ATP using low voltage shock therapy systems include U.S. Pat. Nos. 4,408,606, 4,398,536, 4,488,553, 4,488,554, 4,390,021, 4,181,133 and 4,280,502.
Tachycardia is often the result of electrical feedback within the heart; a natural beat results in the feedback of an electrical stimulus which prematurely triggers another beat. By interposing a stimulated heartbeat (i.e., a pacing pulse), the stability of the feedback loop is disrupted. For example, patients with MVT can often times be successfully paced out of the tachycardia using a rapid burst of high rate pacing. The burst consists of a selected number of pulses all delivered at the same rate, an accelerating rate, or an alternating accelerating/decelerating rate. The mechanism that determines success of the burst is the ability to peel-back the refractories between the pacing site and the origin of the arrhythmia and penetrate the reentrant loop.
In conventional ATP, anti-tachycardia pacing pulses are delivered using two electrodes within the right ventricle (RV). The inventors of the present invention are aware of one study of the efficacy of bi-ventricular (BV) ATP. See Bocchiardo et al., xe2x80x9cEfficacy of Biventricular Sensing and Treatment of Ventricular Arryhthmias,xe2x80x9d PACE, Vol. 23, November 2000, pp. 1989-1991. In the Bocchiardo study, the BV pacing was accomplished using an RV tip electrode, an RV proximal electrode, and an LV tip electrode. The Bocchiardo study concluded that xe2x80x9c[t]he success rates of spontaneous VT termination by BV ATP versus RV ATP were comparable.xe2x80x9d The inventors of the present invention, however, believe that there may be many advantages to BV ATP.
There is a need for improved methods and devices for ATP. More specifically, there is a need to increase the success rate (i.e., decrease the failure rate) of VT termination using ATP. Such improved methods and devices will preferably also reduce the amount of time required to convert a tachycardia to normal sinus rhythm.
The present invention relates to improved methods and devices for performing anti-tachycardia pacing (ATP) to convert a ventricular tachycardia (VT) to normal sinus rhythm. Many embodiments of the present invention relate to the use of bi-ventricular (BV) ATP.
According to an embodiment of the present invention, the first pair of electrodes are shorted together to produce a unipolar electrode. The first anti-tachycardia pacing pulses are then delivered to the left ventricle using the shorted together first pair of electrodes. The first pair of electrodes include, for example, a left ventricular (LV) tip electrode and a LV ring electrode. Similarly, the second pair of electrodes can be shorted together prior to delivering the second anti-tachycardia pacing pulses to the right ventricle (i.e., using the shorted together second pair of electrodes). The second pair of electrodes include, for example, a right ventricular (RV) tip electrode and a RV ring electrode. In another embodiment, the RV tip electrode, the RV ring electrode and a RV coil electrode are all shorted together to produce an even larger electrode. The second anti-tachycardia pacing pulses are then delivered to the right ventricle using the shorted together RV tip, ring and coil electrodes.
An embodiment of the present invention includes sensing a signal using a pair of electrodes implanted in a ventricle of a patient""s heart, and then shorting together the pair of electrodes. Anti-tachycardia pacing pulses are then delivered to the ventricle using the shorted together pair of electrodes. Timing of at least one of the pacing pulses is based on the sensed signal. The pair of electrodes can be a left ventricular (LV) tip electrode and an LV ring electrode implanted in the left ventricle. The pair of electrodes can alternatively be a right ventricular (RV) tip electrode and an RV ring electrode. An RV coil can also be shorted together with the RV tip and RV ring to provide an even larger electrode. The electrodes can be un-shorted after delivery of the unipolar pulses.
In an embodiment of the present invention, the pacing pulses delivered to the right ventricle have an opposite polarity compared to the pacing pulses delivered to the left ventricle.